Role of nitric oxide in the reflex diuresis in rabbits during pulmonary lymphatic obstruction

Abstract

The role of nitric oxide in the reflex diuresis in response to pulmonary lymphatic drainage was examined in anaesthetized, artificially ventilated New Zealand White rabbits. Pulmonary lymphatic drainage was obstructed by raising the pressure in a pouch created from the right external jugular vein. Pulmonary lymphatic obstruction resulted in a significant increase in urine flow from an initial control value of 8.9 ± 0.5 ml (10 min) −1 to 12.1 ± 0.6 ml (10 min)during lymphatic obstruction (mean ± S.E.M.; n = 17, P < 0.001). This increase in urine flow was accompanied by a significant increase in the excretion of sodium. Additionally, renal blood flow remained unchanged during the increase in urine flow caused by lymphatic obstruction. Intravenous infusion of L-NAME, a non-selective inhibitor of nitric oxide synthase (NOS), abolished the reflex diuresis. Furthermore, intraperitoneal administration of the relatively selective neuronal NOS blocker, 7-nitroindazole also abolished the response. It was observed that infusion of a more soluble neuronal NOS blocker, 7-nitroindazole sodium salt (7-NINA), into the renal medulla also abolished the reflex diuresis. These findings suggest that the increase in urine flow in rabbits caused by pulmonary lymphatic obstruction is dependent upon the integrity of neuronal NOS activity within the renal medulla.

Role of adrenergic receptors in the reflex diuresis in rabbits during pulmonary lymphatic obstruction

“…Previous investigations have suggested that the response was mediated by NO produced by n‐NOS in the renal medulla (McCormick et al 2004). The present study has shown that the reflex diuresis is abolished by intramedullary infusions of the α 2 adrenergic receptor antagonist rauwolscine.…”

Role of Nitric Oxide in the Diuresis and Natriuresis Occurring in Patients with Obstructive Sleep Apnoea Syndrome

“…Later on, it was demonstrated that the diuresis was due to generation of renal NO. 33 There are reports which show that the renal NO generation is mediated by activation of alpha-2 receptors. 34 These studies establish that sympathetic excitation can lead to NO generation by activation of nNOS through alpha-2 receptors.…”

Prolonged exposure to inhaled nitric oxide transiently modifies tubular function in healthy piglets and promotes tubular apoptosis

“…We are aware of a number of uncontrolled factors in our protocol. Among them we acknowledge the lack of control of altered neuronal input to the kidneys, which would have necessitated excision of the nerve input to the organ (McCormick et al. 2004); the lack of hormonal control which with altered concentrations can change sodium and water loss as well as retention (Cowley et al.…”